© 1998 by European Society of Cardiology
Copyright © 1998, European Society of Cardiology
Endothelin and heart transplantation
Laboratoire des Régulations Physiologiques et des Rythmes Biologiques chez l'Homme, JE 2105, Institut de Physiologie, Faculté de Médecine, Strasbourg, France
* Corresponding author. Tel: +33-3-8835-8768; Fax: +33-3-8824-3334; E-mail: francois.piquard@physio-ulp.u-strasbg.fr
Received 9 January 1998; accepted 26 May 1998
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1 Introduction |
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Endothelins are 21-amino-acid peptides that are produced ubiquitously by vascular endothelial and smooth muscle cells, but also by numerous other cells in many different organs. Endothelin-1 (ET-1) appears to be the predominantly produced isoform and to be responsible for most of the physiological and pathophysiological changes seen in humans. As suggested by its mitogenic properties, by its potent and long-lasting vasoconstrictor effects and by its origin in vasculature, ET-1 is thought to be mainly a cardiovascular hormone and/or paracrine factor that may play a key role in cardiovascular diseases such as systemic hypertension, atherogenesis, cardiac hypertrophy, heart and circulatory failures [1–5].
To date, although increased circulating ET-1 levels have been reported in heart-transplant recipients (Htx), suggesting a role for ET-1 in the cardiovascular and renal adaptation to human heart transplantation [6, 7], no attempt has been made to review the available literature concerning ET-1 after heart transplantation. We
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2 Endothelin 1 concentrations after heart transplantation |
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3 Pathophysiological significance of ET-1 after heart transplantation |
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3.1 Potential role of endothelin in accelerated coronary artery disease in Htx
3.2 Potential role of ET in acute graft rejection after heart transplantation
3.3 Potential role for ET in the pathogenesis of posttransplantation nephropathy and hypertension
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